Our knowledge of the effects of blast injury dates from the Balkan wars in 1914, when Franchino Rusca, a Swiss researcher, observed 3 soldiers who had been killed by an explosion without evidence of any external in-juries.1 Rusca went on to use rabbits as an animal model and demonstrated that the cause of death was pulmonary embolism. During WWI, blast injury was thought to be a nervous system disorder and labeled "shell shock." (At that time, sychological casualties were lumped together with those who had no visible injuries.)2
In WWII, a noteworthy number of casualties were found among civilians in both German and British cities after bombing raids. "Blast lung" was the term coined for massive pulmonary hemorrhage from disruption of the alveolar architecture and formation of alveolar-venous fistulas resulting in air embolism.3 Following WWII, blast injury was intensively investigated in the United States, due to the perceived threat of nuclear warfare. But it is only since the advent of terrorist suicide bombings that civilian physicians have become significantly concerned about the cause and treatment of blast injuries.2 Unfortunately, the threat of suicide bombing seems to have spread from the Near East to the Far East and back to Europe, as evidenced by both the Madrid and London attacks. The obvious concern is when, not if, the practice will spread to the United States.
Prior to 1995, most civilian emergency physicians in the US had neither experience of nor interest in the effects of explosive devices. This changed abruptly with the destruction of the Alfred P Murrah Federal Building by a truck bomb ? the 1995 blast rocked downtown Oklahoma City and resulted in more than 750 casualties, with 167 fatalities.4 Unfortunately, many smaller devices are exploded each year in the United States.5-7As a result of the casualties associated with September 11, 2001, more US physicians have had to face the specter of explosion and blast injuries filling their own EDs.8,9 The London and Madrid bombings (on July 7, 2005 and March 11, 2004, respectively) have forced physicians in other countries to consider or reconsider their potential roles in explosions and blast injuries due to terrorism.
Bombings are clearly the most common cause of casualties from terrorist incidents.10Recent terror tactics include an increasing use of suicidal/homicidal bombers who deliberately accompany the explosive device (often wearing it) to ensure its maximum effect.11 These bombers have walked or driven into buses, subways, cafes, residential areas, guard posts, and governmental buildings. The use of suicide devices in the US has yet to occur, but given the political climate, the scenario is very likely. Increasingly, information resources, such as the Internet, terrorist training camps, and even library and television sources, have made the knowledge needed to construct these simple and very effective explosive devices readily available.
Research on blast injury is not a new study for those interested in combat medicine. This issue of Emergency Medicine PRACTICEwill review the current literature, including the potential mechanisms of injury, early signs of these injuries, and the natural course of the problems caused by explosive blasts.
AGE - Arterial gas embolism
ANFO - Ammonium nitrate-fuel oil (explosive)
ATF - Bureau of Alcohol, Tobacco, Firearms and Explosives
BLEVE - Boiling liquid expanding vapor explosion
CT - Computed tomography
C-4 - Composition C-4 (explosive)
DPL - Diagnostic peritoneal lavage
FAST - Focused abdominal sonography for trauma
FBI - Federal Bureau of Investigation
HE - High-order explosive
IED - Improvised explosive device
LE - Low-order explosive
PETN - Pentaerythritol tetranitrate (explosive)
RDX - Royal demolition explosive
TATP - Triacetone triperoxide, also called TCAP or acetone
peroxide (non-nitrate high explosive)
TM - Tympanic membrane
TNT - Trinitrotoluene (explosive)
For this review, MEDLINE, Ovid, BestBETs (Best Evidence Topics), Google Scholar, and Google were all searched using the terms blast injury, explosions, bombings, and explosives. The terms were used in Boolean combination and separately in each database, as appropriate.
As might be expected, there were no prospective, randomized, placebo-controlled studies of any treatment. There were, however, multiple retrospective studies, analyses of case reports, animal studies, and many individual case reports and short series. The literature of blast injuries is replete with case reports and data mining from trauma registries. There are few meta-analyses and even fewer prospective studies. This is due partly to the nature of the injury: sudden, random, and unpredictable. Another reason is the dispersion in both time and space of these kinds of injuries. Although recent bombings have had a widespread effect, they generally do not occur in the same location frequently enough to start a randomized study of any treatment methodology. (Figure 1) The exceptions would be England and Ireland in the 1980s and 1990s, and the present-day Middle East, specifically Israel and the US military in Iraq. (All of these exceptions are due to a markedly increased number of bombings in a short period of time in the given locales.) Many of the case reports cited in this article are from researchers in England, Israel, and the United States military. There are no evidence-based ATLS data about bombings and explosive injuries. The military has trauma registries, but this information is not open to public scrutiny. There is a published summary of the joint US Navy-Marine Corps Combat Trauma Registry available at http://www.stormingmedia.us.
An explosion is an event that occurs when a substance rapidly releases energy and produces a large volume of gaseous products. High-explosive, thermobaric, and nuclear detonations all provide this change in potential energy to kinetic injury in a very short period of time. The extreme compression of molecules by this change in energy creates the blast wave that moves outward from the epicenter of the blast. These blast waves travel faster than the speed of sound. Blast products ? gas, particles, debris of the container, and items in proximity to the explosive (including human remains) ? also spread outward, but travel much more slowly. Both the blast wave and the blast products can cause injuries as described below.
Trauma caused by explosions traditionally has been categorized according to the following scheme: injury caused by the direct effect of the blast wave (primary injuries); effects caused by other objects that are accelerated by the explosive wave (secondary injuries); effects caused by movement of the victim (tertiary injuries); and miscellaneous effects caused by the explosion or explosives (sometimes termed quaternary injuries). (Figure 2)
The injury pattern following an explosion is partly random. Explosions have the potential to cause multisystem injuries involving multiple patients simultaneously. The trauma that results from an explosion depends on the combination of the size of the explosive charge, the nature of the explosive, the container and surrounding or contained items, any shielding or protective barriers between the victim and the explosion, the surrounding environment, the method of delivery, and the distance between the explosion and the victim.
A conventional explosion is the rapid chemical conversion of a solid or liquid into gas. Thermobaric explosives (commonly called fuel-air explosives) are either gases mixed with air or finely divided particles or droplets suspended in air. Explosives are categorized as either high-or low-order, and they cause somewhat different injury patterns. The explosive effects of nuclear weapons will not be discussed in this article.
High-order explosives (HE) are chemical materials that have an extremely high reaction rate. This reaction is often called a detonation.(Table 1)
When a high explosive detonates, it is converted almost instantaneously into a gas at very high pressure and temperature. For example, the major ingredient in composition C-4 or RDX (cyclotrimethylenetrinitramine) can generate an initial pressure of over 4 million pounds per square inch (4x106 psi).12 These high-pressure gases rapidly expand from the original volume and generate a marked pressure wave ? the "blast wave" ? that moves outward in all directions. The result is a sudden, shattering blow on the immediate surroundings.
High explosives are further categorized as primary and secondary high explosives. The primary-high explosive is very sensitive, can be detonated very easily, and generally is used only in primary and electrical detonators. Secondary high explosives are less sensitive, require a high-energy shock wave to achieve detonation, and are generally safer to handle.
The blast wave refers to an intense rise in pressure ? often called "overpressure" ? that is created by the detonation of a high explosive.2 A typical pressure wave from a high explosive explosion in air is shown in Figure 3.
The blast wave transfers energy to objects or bodies in its path. The extent of damage due to the pressure wave is dependent on:
As shown in Figure 4, the blast wave has 3 components:
In air, the peak pressure is proportional to the cube root of the weight of explosives and inversely proportional to the cube of the distance from the detonation.
This shock wave can be so abrupt that it shatters materials. This effect is termed brisance (the measure of the rapidity with which an explosive develops its maximum pressure) ? a quality that varies from high explosive to high explosive. When craters are formed at the site of an explosion, this shock wave has disintegrated the material close to the explosion. Because the explosive gases continue to expand outward, the pressure wave rapidly deteriorates into an acoustic wave. Until the wave deteriorates enough to completely engulf the body simultaneously, tissue damage will depend on both the magnitude of the pressure spike and the duration of the force (represented by the area under the curve).
A blast wave that would cause only modest injury in the open can be lethal if the victim is in a confined area or near a reflecting surface, such as a solid wall or a build-ing.2 If the pressure wave is near a solid barrier, the pressure exerted at the reflecting surface may be many times that of the incident blast wave.
For a single, sharp rising blast wave caused by detonation of a high explosive, the damage to human structures is a function of the peak pressure and the duration of the initial positive phase. The greatest energy transfer occurs at points where tissue density changes. Energy transfer at a bone/soft tissue interface may partially amputate limbs.13 Figure 5 illustrates the estimated blast levels needed to cause damage in humans.
Blast wind refers to the rapid bulk movement of air and other gases from the explosion site. It occurs with both low-order and high-order explosives. Some explosives are manufactured to produce a relatively low-energy blast wave, but large amounts of gaseous products. These explosives produce a sustained blast wind and localized heaving with minimal blast. They are particularly useful in mining and demolition projects.
Low-order explosives are designed to burn and subsequently release energy relatively slowly. These explosivesare often called propellants, because their most common use is to propel a projectile through the barrel of a weapon.The principle military uses for low-order explosives are as propellants and in fuses. Typical improvised low-order explosives include pipe bombs, gunpowder, black powder, and petroleum-based bombs, such as Molotov cocktails or gasoline tankers. Since low-order explosives do not form shock waves, they do not have the quality of brisance.
The process of rapid, progressive burning of a loworder explosive is called deflagration. This burning takes place so slowly that when the low-order explosive is set off in the open, the gases push aside the air with only a flame and no appreciable disturbance. If the low-order explosive is confined, the speed of the reaction is markedly increased, but does not approach that of a high-order explosion. The explosion has more of a pushing effect than a shattering effect (ie, blast wind without a blast wave).
The explosion from low-order devices lacks the overpressure wave; thus, injuries are due to ballistics (fragmentation), blast wind from the expansion of the gases, and thermal injuries from the heat of the explosion. Obviously, it is clinically impossible to tell whether fragment wounds have occurred because the fragment was propelled by a high-order versus a low-order explosive. Likewise, if the victim is flung by a blast wind into a structure, it matters little to either the patient or the clinician that the explosion occurred from detonation of a high-order explosive or deflagration of a low-order explosive.
In this explosive device, a substantial quantity of fuel is vaporized and mixed with air. Fuel-air explosives represent the military application of the vapor cloud explosions and dust explosion accidents that have long plagued a variety of industries. Firefighters are all too familiar with the explosive effects of this device. (Table 2)
Since these explosive mechanisms are not uncommon in the civilian world, the emergency physician needs to know the special effects of this form of explosive. An astute terrorist could use these mechanisms to create a massive explosion.
In the military device, mixture of the fuel with air over the target may be accomplished by a dispersal charge. After the munition is dropped or fired, the first explosive charge bursts open the container at a predetermined height and disperses the fuel in a cloud that mixes with atmospheric oxygen (the size of the cloud varies with the size of the munition). The cloud of fuel flows around objects and into structures. After the fuel and air are mixed, a second detonation provides the spark needed for ignition.
There are dramatic differences between explosions involving fuel-air mixtures and high explosives at close distances. The shock wave from a trinitrotoluene (TNT) explosion is of relatively short duration, while the blast wave produced by an explosion of fuel-air mixture displays a relatively long duration. The duration of the positive phase of a shock wave is an important parameter in the response of structures to a blast. The temperature can be as high as 3000?C ? more than twice that generated by a conventional explosive. The blast wave can travel at approximately 10,000 feet per second.
The blast effects from vapor cloud explosions are determined not only by the amount of fuel, but more importantly by the combustion mode of the cloud. Most vapor cloud explosions are deflagrations, not detonations.15 Flame speed of a deflagration is subsonic, with flame speed increasing in restricted areas and decreasing in open areas.
Flame propagation speed has a significant influence on the blast parameters, both inside and outside the source volume. High flame front speeds and resulting high blast overpressures are seen in accidental vapor cloud explosions, where there is a significant amount of confinement and congestion that limits flame front expansion and increases flame turbulence. These conditions are more difficult to achieve in the unconfined environment in which military fuel-air explosives are intended to operate.
Since the fuel uses up the atmospheric oxygen, asphyxia for those who are not immediately killed by the explosive device can be a problem. Likewise, since the temperature of the burning fuel is greater than that of conventional explosives, extensive burns can occur in survivors.
Charles Edward Munroe coined the term "The Munroe Effect" in 1885. He noted that a high explosive with a cavity facing a target left an indentation. The earliest known reference to the effect appears to be 1792, and there is some indication that mining engineers may have exploited the phenomenon over 150 years ago. A typical shaped charge consists of a solid cylinder of explosive with a conical hollow on one end, lined with a dense ductile metal, such as copper. (Figure 6) When detonated from the other end, the force of the explosive detonation wave is great enough to project the copper into a thin, effectively liquid stretching that has a tip speed of up to 12 km/sec. The enormous pressures generated cause the target material to yield and flow plastically.
Explosively formed projectiles (EFPs) are related to shaped charges, but form a fragment rather than a jet. A computer-designed, dish-shaped metal liner is placed in front of a shaped explosive charge. These explosive devices with wide-angle cones and other liner shapes, such as plates or dishes, do not jet, but instead give an explosively formed projectile. (Figure 7) When the explosive is detonated, the shock wave deforms the liner in a preset way to create a symmetric projectile traveling at very high speeds. Varying the liner shape and explosive confinement changes the shape and velocity. These sophisticated devices have been used in Iraq against Allied forces. They routinely defeat armor and can cause significant injuries.(Figure 8)
Explosive devices may also be characterized based on their source. The Bureau of Alcohol, Tobacco, Firearms and Explosives (ATF) categorizes explosives into "manufactured" and "improvised." A "manufactured" explosive implies a standard, mass-produced, and quality-tested weapon. "Improvised" describes the use of alternative materials, weapons produced in small quantities, or a device that is used outside of its intended purpose. Improvised explosive devices (IEDs) may be professional in appearance, and their operation may be quite lethal, if designed by someone with training in explosives. (Note that by this definition, any experimental explosive device is an improvised" device, since it is not set to standards, mass-produced, and quality-tested. This rather unwieldy definition encompasses all experimental military devices produced by professional arms manufacturers.)
Improvised explosive devices (and many military munitions) can be triggered in a variety of ways, including electronic transmitters and switches, tilt switches, thermal switches, and various types of motion detectors. Improvised weapons vary in quality of the explosive used,from commercial explosives, TNT, Semtex, C-4, ammoniabased fertilizer, and fuel oil (used widely as an industrial explosive) to a simple, match-filled pipe bomb. High-quality IEDs may resemble military weapons in effect and appearance. The variety of initiation methods, explosive fillings, and fabrication techniques creates a threat that can be quite daunting to the professional explosive ordinance disposal crew.
Recent improvised devices have been manufactured with nonnitrogen explosives (TATP) in order to defeat explosive sniffing devices and dogs. These nonnitrogen explosives are often quite unstable and may spontaneously detonate ? this means that, no matter how innocuous an improvised device may appear, the amateur should never touch the device.
Another important factor that defines blast injury patterns is the medium in which the blast occurs. An underwater blast wave causes far more damage, because water is essentially incompressible.2,16 A wave resulting from an underwater blast travels farther and moves faster than a wave from a similar explosion in the air. Blast injuries in water occur at greater distances and may be much more severe.17,18 Personnel treading water are at higher risk for abdominal than thoracic injury from an underwater explosion. Fully submerged victims are at equal risk of combined thoracic and abdominal blast injuries, but the blast injury occurs at 3 times the distance from the underwater explosion.19
Another characteristic of blast waves is that they are indeed true waves. (Figure 3 on page 4) The injury patterns they produce are not only related to the medium through which they travel, but the position of the victim's body in relation to reflecting or deflecting objects that the wave strikes. For example, explosions near or within hard, solid surfaces become magnified 2-9 times as the shock wave is reflected.20 In fact, victims located between the blast and a building generally suffer 2-3 times the degree of injury that an individual in an open environment would receive.21
Blast injury has an overall lethality of about 7.8% in open air; this jumps to 49% when the blast occurs in a confined space. One meta-analysis reported a 70% incidence of minor soft tissue injuries.21 Traumatic amputations will occur in about 11% of cases. Traumatic amputations serve as a marker of severe multisystem trauma and subsequent high mortality.13 The World Trade Center was an exception in that most victims had either few injuries or died as the building crashed down on them.
Primary blast injuries are caused only by high explosives and are due to the direct effects of the blast wave on the human body. (Since low-order explosives do not form a supersonic blast wave, they cannot cause primary blast injury. This is the sole clinical difference between wounds caused by a low-order explosive and a high-order explosive.)
The overall incidence of primary blast injury in soldiers in combat is about 5%.22 Cernak retrospectively examined the records of 1303 patients and found evidence of primary blast injury in 51% of admitted patients.23 (The victims of primary blast injury almost always have other types of injury, such as penetrating wounds from flying debris or blunt trauma from impact on immovable objects).23
Damage from an explosion (Table 3) depends upon:
In World War II, blast overpressures were thought to gain access to internal organs through natural orifices.24 This has since been proven inaccurate. Other, more recent theories that have been proposed include implosion of gascontaining structures, inertial effects on tissues of different
densities, and spalling at water-gas interfaces.
The most likely mechanism of primary blast injury that fits current modeling techniques is the irreversible work effect related to the differences in tissue tensile strength and speed of the blast wave through the different tissues. This is currently thought to be the major cause of primary blast injuries.25 The onset of damage occurs when the blast wave compresses the tissues. The resulting forces exceed the tensile strength of the material and cause shearing of vascular beds, pulmonary contusions, and gastrointestinal hemorrhages as the tissues are compressed and expanded.26,27
The illustration often used is of an aluminum can that is dented slightly and pushed back into shape. When the can is stressed beyond its tensile strength, it can no longer be restored to its original shape.28
Some combination of stress and shear waves is likely in all nonpenetrating blast trauma. Stress that exceeds tissue tensile strength probably predominates when blast surface loading exceeds velocities of 80-90 m/sec.25
Primary blast injury is common in the ear, the respiratory tract, and the gastrointestinal tract. Of the 3 organ systems, the ear is the most easily damaged.
While the ear is the most easily damaged organ system in primary blast injury, it is also the easiest to protect. The structures of the ear are designed to collect and magnify sounds, so that the tympanic membrane will move with the sounds. Unfortunately, they also collect and magnify pressure waves. At a pressure of about 35 kilopascals (5 psi), the human eardrum may rupture. With an overpressure of 100 kilopascals (14 psi), almost all eardrums will be ruptured. The eardrum most frequently ruptures into the inferior pars tensa. At lesser pressures, the overpressure may cause hemorrhage into the drum without a rupture. With extremely high pressures, the drum may be destroyed and the ossicles dislocated or fractured.29 Rupture of the eardrum will cause pain, hearing loss, and possibly tinnitus. Eardrum perforations, hearing loss, and dizziness may interfere with daily activities and may have a telling effect on the individual's quality of life.29
Physical examination may reveal blood in the external canal. Examination of the tympanic membrane with an otoscope may show evidence of the perforation or of a hematoma of the tympanic membrane.
It is often held as gospel that rupture of the tympanic membrane is a marker for serious gastrointestinal or pulmonary injury. If the patient has ear protection, this may not be the case. Likewise, if the patient is in the water, but with their head out of the water, the tympanic membranes may not be exposed to an underwater blast wave. Even in those exposed to simple blast injury, isolated eardrum rupture does not appear to be a good marker of concealed pulmonary blast injury or poor prognosis.30 Auditory barotrauma is quite common in blast injuries. In the Oklahoma City bombing, the incidence of auditory injury was 35%.4,31 This does not include those patients with partial, temporary hearing losses or those who complained of tinnitus for an extended period of
time.29
The lungs are particularly susceptible to damage due to the extensive air/lung tissue interfaces. Blast lung is a direct consequence of the supersonic pressure wave generated by a high explosive.32 It is the most common fatal injury caused by the primary blast among the initial survivors of the explosion. These lung injuries may not be apparent externally or immediately, but may lead to death if not diagnosed and treated promptly. An overpressure of about 40 psi will cause lung injuries.
Pulmonary blast effects in survivors have been described as rare in the British literature, but are observed more often in the Israeli experience, with enclosed explosions that occur on a bus.33,34
Damage to the lungs can include pulmonary contusions and/or pulmonary barotrauma, such as pneumothorax, pulmonary interstitial emphysema, pneumomediastinum, or subcutaneous emphysema. The most common lung injury associated with a blast wave is a pulmonary contusion.35,36 This may take the form of microhemorrhages with perivascular/peribronchial disruption. It appears to be more common on the side closest to the explosion, but this may be influenced by the geometry of the surrounding area and reflected energy.35-37 The alveolar wall may be torn, causing a blood-filled emphysematous change to the lung and subsequent hemoptysis. Pulmonary contusions may develop with or without a pulmonary laceration.
It should be assumed that if a patient is wheezing after a blast injury, then this wheezing is due to a pulmonary contusion. Other causes of wheezing may be pulmonary edema from myocardial contusion or infarction, or exacerbation of underlying disorders, such as asthma or COPD. If the patient has hemoptysis after a blast injury, the clinician must entertain a high suspicion for pulmonary blast injury.
Pulmonary contusions impair gas exchange at the alveolar level. The changes seen on microscopic examination closely resemble the pulmonary contusions seen in nonpenetrating blunt chest trauma. The histologic appearance of lung damage by blast overpressure is dominated by hemorrhage into the alveolar spaces. The degree of respiratory insufficiency depends on the magnitude of hemorrhage into the lung.
Parallel thoracic ecchymoses, once thought to be along the ribs, may be seen with larger blast loads.28,36 These ecchymoses parallel the intercostal spaces. Rib fractures may occur due to blast injury, but are much more likely to be due to secondary or tertiary blast injury mechanisms, at least in survivors.35,38 The patient may have minimal or no symptoms initially. Blast lung is clinically characterized by the triad of dyspnea, bradycardia, and hypotension. The clinician should suspect blast lung in any victim who presents with dyspnea, cough, hemoptysis, or chest pain following blast exposure. Signs of blast lung are usually present at the time of the initial evaluation, but have been reported as late as 48 hours after the explosion occurs.
The occurrence of late pulmonary symptoms in primary lung blast injury has recently been questioned
by Pizov et al, who described 15 patients with primary lung blast injury.38 All of the patients required intubation and ventilation, either at the scene of the explosion or on admission to the ED. No patient in their series developed blast lung that did not require ventilatory support within the first 6 hours after the injury. It should be noted that all of the patients in this series were victims of blast injury within the enclosed confines of a "bus bombing." As noted earlier, blast pressures within enclosed areas are often
much higher.
The overpressure may cause pulmonary barotrauma, including pneumothorax or pneumomediastinum. (See Figure 9 for an illustration of pulmonary injury mechanisms.) The patient may develop pulmonary interstitial emphysema, subcutaneous emphysema, and systemic air embolism with larger blast loads.26-28,39 Significant bronchopleural fistulae may lead to air embolism. Air emboli may present in a variety of ways, including shock, myocardial infarction, spinal infarction, or cerebrovascular accident. (See Table 4 for correlation of severity and injury frequency.)
A simple frontal chest x-ray is diagnostic for most cases of pulmonary barotrauma from blast. (Figure 10) Blast lung produces a characteristic "butterfly" pattern on chest x-ray. The pulmonary injuries found
may range from scattered isolated petechiae to confluent pulmonary hemorrhages. The radiographic evidence of pulmonary injury usually begins within hours of the explosion and begins to resolve within 1 week.40
Gastrointestinal injuries were once thought to occur with the same frequency as lung injury. A recent, large Israeli case series found that abdominal injuries were seen only with massive trauma.33 In this series, all of the patients tenesmus. Blast injury to the gastrointestinal tract should be suspected in anyone who has abdominal pain, nausea, vomiting, hematemesis, rectal pain, testicular pain, unexplained hypovolemia, or any finding compatible with an acute abdomen after exposure to an explosion.
The clinician should be aware that the abundant highvelocity fragments associated with recent suicide bombs may also cause intraabdominal injuries. These injuries can certainly include penetrating bowel injuries.45 Initial symptoms of penetration are the same as outlined above.
Primary blast injury can cause concussion or traumatic brain injury, although this finding is difficult to distinguish from the concussion due to impact with another object. Likewise, high-velocity fragments can penetrate the skull. The clinician should be quick to consider CT or MRI in these patients.
Although the heart is well protected and not subject to the air/fluid shear of primary blast injury, myocardial contusion can lead to either arrhythmia or hypotension.25
Secondary blast injury is caused by the bomb fragments and other debris propelled by the intense energy release of an explosion. (These fragments are often erroneously referred to as "shrapnel." Shrapnel is actually the name for an artillery round containing multiple spherical projectiles and an explosive charge. This antipersonnel projectile was designed in 1784 by Major-General Henry Shrapnel, an English artillery officer. The round essentially functions as a very large shotgun, with several hundred half-inch lead balls.) As distance from the blast epicenter increases, the effect of the blast itself is reduced, and the effect of fragments and debris propelled by the explosive becomes more important. Conventional military explosives may create multiple fragments, with initial velocities of up to 2500 m/sec (8202 feet per second).46 (In comparison, the very fast-moving M-16 round has a muzzle velocity of 853 meters (2800 feet) per second.)47
These flying projectiles can produce both penetrating and blunt trauma, depending on the size of the projectiles and the speed at which they travel. With these velocities, the victim does not have to be in close proximity to the explosion. Individuals far from the scene of an explosion can be struck and injured by this debris. After the 1998 terrorist bombing of the US Embassy in Nairobi, flying glass wounded victims up to 2 kilometers away.25 For US Air Force personnel wounded in the Khobar Towers in 1996, 88% of patients were injured by flying glass.48 (The reason for the "stand-off distances," noted in Table 5, is to decrease to acceptable limits the number of injuries that occur from flying debris when the bomb explodes.) The farther away the explosion occurs, the less serious the injury.
Terrorist devices often have additional objects, such as nails, nuts, and bolts, added to the explosive mixture in order to increase the effects of secondary blast injury. (Figure 11) These fragments are of high mass and kinetic energy and the damage that they inflict at close range is considerable. Military devices, such as shells and grenades, may be designed in such a way as to increase the number of fragments flung by the explosion.
Secondary blast injury is much more common than primary blast injuries. Indeed, secondary blast injury is the most common cause of death in blast victims. The penetrating injuries occur most often in the exposed areas, such as the head, neck, and extremities. (Figure 12) Thoracic and intraabdominal injuries may occur when fragments penetrate.45 (Figure 13) Glass causes many of the secondary blast injuries (up to 50% of all blast injuries). Victims who are peppered with glass are often difficult to distinguish from victims who are peppered with glass and have penetrating injuries.49 The clinician must be suspicious of any penetrating torso or abdominal injury.
Secondary blast injuries may not be initially obvious. A seemingly small abrasion or wound may mask the entrance wound for a substantial fragment.
Up to 10% of blast survivors will have significant eye injuries.50 (Figure 14) These injuries may be perforations from high-velocity projectiles. Glass is notorious for causing these ocular injuries. While window fragments are not often lethal, they can cause blindness and ruptured globes. At the speeds at which explosively propelled fragments of glass travel, there is no time for the blink reflex to operate. These injuries can occur with minimal initial discomfort and can present days after the event. Symptoms include eye pain and irritation, foreign body sensation, alterations of vision, periorbital swelling, or periocular contusions. Signs can include loss of vision, decreased visual acuity, globe perforation or rupture, lid lacerations, and subconjunctival hemorrhage around the point of entry.
Tertiary blast injuries are caused when the victim's body is propelled into another object by the blast winds.28,51 Tertiary effects result from the bulk flow of gas away from the explosion. Blast winds can generate a body acceleration of over 15 g's. They most often occur when the victim is quite close to the explosion.
This displacement of the victim can take place relatively far from the point of detonation if the victim is unfortunately positioned in the path that gases must take to vent from a structure, such as a doorway, window, or hatch. Likewise, if the patient is in an alley, magnification of the blast wind may occur due to the configuration of the buildings.
It is the deceleration caused by impact into a rigid structure that causes the majority of injuries. A person who is flung into a fortified immovable object with a velocity greater than 26 ft/sec will have a mortality rate of about 50%.52 The most common injuries are fractures and closed head injuries. Isolated body parts may be broken, dislocated, or even amputated. Injuries from this mechanism also depend on what the victim hits in the environment and can range from simple contusions to impalement. Victims may also tumble along the ground, sustaining abrasions, contusions, and "road rash."
This category of blast trauma includes burns from fire or radiation, crush injury associated with structural collapse, poisoning from carbon monoxide or other toxic products of the explosion, and inhalation of dust or chemicals from the explosion. This category would include the burns sustained from thermobaric weapons.
The unprotected human body can survive a blast with a peak overpressure of 30 psi, but buildings and other structures collapse with stress of only a few psi. (Table 3) This means that people can survive the effects of a blast, only to be injured by collapsing buildings.
The blast may be a vector for both chemical warfare agents and biological warfare agents. The effects of these agents on the body may well overshadow any effects from the explosive energy.
Patients who have been exposed to a blast in an enclosed area should have carboxyhemoglobin levels obtained. Inhalation of irritant gases or dusts may also trigger wheezing or even delayed pulmonary edema in these patients.
The job of the prehospital provider confronted with a major explosion becomes extremely difficult. The emergency services provider needs to ensure appropriate on-scene management, including triage, transportation to medical care, and appropriate distribution to hospitals with both facilities and skills to care for the victims. There may be additional problems due to unsafe or collapsed buildings, the dangers of further explosions, and civilian panic.10
An explosion that occurs in a confined space (including vehicles, mines, buildings, and subways) is associated with greater morbidity and mortality. If the structure collapses, this markedly increases the mortality associated with the event (assuming that there are people in the structure).
The early presentation of victims can be deceiving, because the initial manifestations of significant blast injury can be subtle. Blast lung injury is the most common fatal injury among initial survivors of the blast.53
The prehospital provider can aid the preparation of the hospital for reception of the victims by giving a preliminary needs assessment for the hospital(s). Identification of the site of the explosion is particularly helpful. Terrorist targets tend to be highly visible and may play an important operational or symbolic role in the community. The site also suggests the number of potential victims that may be involved. The location establishes the proximity to the hospital and the potential for those injured to arrive at the hospital within a few minutes by alternative transportation. Mutual aid agreements and location of the explosion may dictate transportation to other hospitals. Further information about the delivery system in a terrorist attack and whether the explosion occurred in open air or a confined space may help estimate needs for other resources.
If the blast casualty is ambulatory, it is critical to minimize physical activity. Exertion after blast injury can markedly increase the severity of the primary blast injury. This was seen in WWII, when some blast casualties appeared well, but died after vigorous activity.54
The EMS provider should be wary of secondary (and, on rare occasion, tertiary) devices and explosions. Foreign experience has shown that terrorists often will set a second device timed to explode some 30 to 100 minutes after the first device has detonated.55,56 This second device is designed to injure EMS, fire, and police personnel who may be at the scene. This second device may often be larger than the first. In some cases, the perpetrator of the explosion may be watching over the area of the explosion, and will either remotely detonate the second explosive or employ high-powered rifle fire to injure or kill responders.
Remember to check all victims for weapons, booby traps, and explosives. It is quite common for a bomber to become a victim of his own device.
Fatal injuries can occur due to blast effects involving the head, chest, and abdomen and are often seen in victims who are close to the detonation.57 Indeed, close to the site of the blast, parts of the victim (or perpetrator) can become missiles that kill or wound other victims.58 Immediate death may occur from massive pulmonary bleeding with rapid suffocation, despite good care. The patient may develop a massive air embolism, may sustain a significant brain injury, or may suffer a traumatic amputation and
exsanguinate before help arrives. Finally, the patient may have a crush injury or impalement injury that causes rapid death before extrication can occur.
The field physician or paramedic should consider a
patient dead in the field when there is:
CPR at the scene is never indicated. There will be too many injured, not enough medical providers, and no significant chance of successful resuscitation in this blunt trauma patient.
Finally, evacuation from the blast site to medical care can be problematic. The blast that caused the injuries may also degrade routes to and from the site of the explosion. Air transport can pose special problems. The barotrauma that results from primary blast injury can be exacerbated by air evacuation. Pneumothorax and arterial gas emboli will enlarge with ascent. Regardless of the altitude and distance of the flight, casualties with field evidence of pneumothorax must have a chest tube placed. Evacuation
aircraft should fly at the lowest possible altitude. Evacuation by long-distance, high-altitude flights should be avoided. Evacuation aircraft should be pressurized to at least 8000 feet (preferably 5000 feet).
If the victim has marginal oxygenation (PO2 <60 mm Hg), the clinician should recognize that oxygenation will worsen with ascent in an aircraft (with the increase in altitude and subsequent decreased barometric pressure) and consider intubation prior to transport.
The first priority of the emergency physician faced with the aftermath of an explosion is to activate the hospital's external disaster plan. During the period before the arrival of the first patients, the physician should clear the ED of all possible patients by either discharge or admission. The administration should simultaneously cancel all elective surgery cases, clear the recovery room, and clear as many intensive care beds as possible.
If your hospital is close to the explosion, expect that the most severely injured patients will arrive after the less injured. The less injured often skip EMS and proceed directly to the closest hospitals.4 For a rough prediction of the "first wave" of casualties, double the first hour's casualty count.
Remember that a secondary device may be employed that can cause substantial additional casualties to include EMS, fire, police, and media.
Most casualties within the injury radius of a conventional explosive detonation or deflagration will have common penetrating, blunt, and burn injuries that are managed no differently than similar nonblast trauma.59 Much of this trauma will be soft tissue, orthopedic, or head injuries.31,60,61 The first and most important step of management is assessment of life support needs and ensuring that the patient has an adequate airway, appropriate ventilation, and adequate circulation. Identify and correct life-threatening external hemorrhage at once. Arrhythmias (particularly bradycardia), hypotension, and apnea are frequently observed after blast injury to the thorax and have been associated with primary blast wave effects on the myocardium and vagal stimulation.3,62
A thorough physical examination should then be performed. The emergency physician should look for sentinel signs of potentially significant blast exposure. (Table 6)
Unfortunately, when the health care provider is faced with dramatic injuries, such as amputations, fragment injuries, and multiple critically ill patients, it is altogether too easy to miss the subtle signs of blast injury. If the clinician overlooks the possibility of primary blast injury, this may further complicate the patient's care.
In addition to the usual questions about medications, allergies, tetanus immunization, prior surgeries, and past/cur-rent illnesses, there are specific questions that may guide your management of the patient who has been near an explosion.
Can you hear me? Do you have ear pain? Tympanic membrane rupture and temporary hearing loss is common in blast injury, but should not be life-threatening (that is, unless the casualty cannot hear life-saving commands or communications!).
Are you short of breath? Do you get short of breath with walking? A pulmonary contusion will inhibit oxygen diffusion and will cause dyspnea. Pneumothorax and hemothorax can decrease the volume of inspired air, with resultant subjective dyspnea. Shock from other causes can give the sensation of dyspnea caused by lactic acidosis from poor tissue perfusion. The more exertion required to elicit dyspnea, the less likely that there is a lung injury.
Do you have pain in your chest? Chest pain may occur from penetrating or blunt trauma, pneumothorax, pneumomediastinum, or myocardial ischemia or infarction due to coronary AGE.
Do you have nausea, abdominal pain, urge to defecate, or blood in your stools? Penetrating or blunt abdominal trauma can cause pain, or the patient may have primary blast injury to gas-filled abdominal organs, ruptured colon, or small bowel.
Do you have eye pain or problems with your vision?
Evaluate the patient for blunt or penetrating eye trauma.
Attempt to determine the distance from the explosion for each patient and whether the victim was in the open air or in an enclosure during the blast. Distance obviously decreases the risk of primary blast injury (at least in the open). Sharing a confined space with an explosion, including the inside of a vehicle, increases the magnitude of the blast wave to the victim. If the patient was in water, this should be noted, and the suspicion for intraabdominal blast injury heightened. If the patient was wearing body armor, this should be noted in the record. While body armor provides significant protection against fragment injuries, it also increases the chance and severity of primary blast injury.63
All injured survivors need to be evaluated with suspicion of primary blast injury. A full set of vital signs is essential and must include the pulse oximetry in all patients. These vital signs should be repeated frequently, as deterioration of the patient may occur over relatively short time periods. This deterioration may be from occult injury to either pulmonary or abdominal pathology. The subtle findings
of tachycardia and a narrowed pulse pressure may be the first signs of this pathology. Signs of specific pathology are found in Table 7.
There are only a few screening studies that are of any benefit in the casualty with primary blast injury.
Pulse oximetry may indicate some degree of lung injury. A falling pulse oximetry should prompt additional monitoring and raise suspicion of pulmonary injury or shock from another injury. With multiple casualties, continuous pulse oximetry may not be possible in all patients. Serial hemoglobin determinations are useful in select cases where internal hemorrhage is suspected. The data may be used as a guide for blood transfusion requirements. Victims of major trauma should have baseline
blood counts, hematocrit, hemoglobin, and crossmatching for potential transfusion. Although most casualties with primary bowel injury have bleeding, it is usually gross hematochezia. A guaiac
positive stool can indicate occult penetrating, blunt, or blast trauma to the bowel.
An immediate chest x-ray should be obtained in all patients who have been near a significant explosion. The clinician should look for evidence of pulmonary contusion (as noted above) and barotrauma. A chest x-ray may also show free air under the diaphragm, signifying hollow viscus rupture in the abdomen from primary blast injury.40
Puncture wounds should be presumed to be due to high-speed missiles and examined accordingly. Any puncture wound of the thorax, abdomen, or extremities should prompt a radiograph, at least. In many cases, CT may be more appropriate.
A CT of the head, chest, or abdomen should be obtained if the history or physical examination suggests pathology in these areas. If the patient is or was unconscious, these CT studies are not optional.
Unfortunately, the CT scanner may also be the biggest bottleneck in the treatment of multiple patients with blast injuries.64 After the Oklahoma City bombing, 19% of 338 patients treated in the ED had CT scans.4 The CT scan is often slow and requires contrast use and equipment availability. Often, CT scanning requires transport away from the emergency care area.
The emergency physician must prioritize CT scans based on the urgency of finding a remedial problem in a survivable patient. A dedicated radiologist and a resuscitation team in the CT scanner suite can both obviate the problems associated with moving the patient from an emergency care area and expedite the movement of patients through the CT scanner suite.
Sonography has become an extension of the physical examination of the abdomen and should be performed whenever available and when abdominal injury is suspected. Focused abdominal sonography for trauma (FAST) aids in the prioritization of penetrating injury patients for the operating room, indicates which cavity to open first in patients with thoracoabdominal injuries, identifies pericardial fluid, and may assist in the diagnosis of hemopneumothorax and hemopericardium.
The 3.5- to 5-MHz curved probe is optimal for the performance of the FAST examination. The abdomen is examined through 4 standard sonographic windows. A FAST examination assists the surgeon in determining the need for laparotomy in blunt-injured patients, but it does not identify specific injuries. A FAST examination does not identify or stage solid organ or hollow viscus injury, but reliably identifies free intraperitoneal fluid.
Hypotension in blast injury victims can be due to several mechanisms:
The patient's fluid volume should be supported without excessive fluid replacement. Too much fluid replacement can, of course, cause increased respiratory distress. Often blood products or colloid solutions are more appropriate in the acute trauma patient than crystalloid infusions.
There is no specific treatment for blast-related ear injuries. The physician should caution the victim to avoid any further auditory injury, if possible. The patient should be transferred to a quieter environment, where available, and the ears should be evaluated within 24 hours.
Debris should be gently removed from the external canal. Neither antibiotics nor ear drops are recommended, particularly if the patient has a ruptured tympanic membrane.65 Tympanoplasty is reserved only for failures of conservative therapy.65 In at least 1 retrospective study of 147 patients, nearly 70% of perforated tympanic membranes healed within 10 months.65
Blast lung is treated by correcting the effects of barotrauma, if any are found. If available, supplemental oxygen should be started on any patient who does not have or cannot maintain a normal oxygen saturation, or those who have any external injuries. Those patients with significant respiratory distress or hemoptysis should have an endotracheal tube placed. This is not without its hazards, however. The provider should opt for the least invasive measure that will still provide appropriate airway support in these patients.66
In one study using thoracic CT scans of patients with pulmonary contusion (not blast injury), patients with less than 18% contusion did not require intubation or ventilation.67 Patients with more than 28% contusion alwaysrequired ventilation. Although this was a small study, the findings are persuasive.
Positive pressure ventilation markedly increases the possibility of both air embolism and pulmonary barotrauma.21,38,68 Avoid positive end-expiratory pressure (PEEP) and high ventilation pressures.66 Preventative strategies include using limited peak inspiratory pressures, pressurecontrolled ventilation, high-frequency jet ventilation, and permissive hypercapnia.10,38,52,68
Because the combination of positive pressure ventilation and blast lung injury poses such a high risk for tension pneumothorax, some authors suggest bilateral prophylactic chest tubes after intubation.69 If the patient needs air evacuation, this becomes an important consideration. If a patient with a blast lung injury abruptly decompensates, the clinician should presume that the patient has a tension pneumothorax and treat accordingly.
Experimental techniques, such as high-frequency jet ventilation or nitric oxide, do not seem to confer any particular benefit to victims of blast lung.38 The use of extracorporeal circulation is associated with catastrophic pulmonary hemorrhage.70
Data on the short- and long-term outcomes of patients with pulmonary blast injury are currently limited. In a retrospective review of 11 patients, Hirshberg et al found that, if the patient survives the blast lung and other trauma, there is a good chance that they will regain full lung function within a year after the injury.71
Arterial gas embolism (AGE) may be the most common cause of rapid death in initial survivors. It often occurs when positive pressure ventilation is started.24,25,39 Symptoms of an air embolism depend on where the bubbles lodge. Air embolism can present as stroke, MI, acute abdomen, blindness, deafness, spinal cord injury, or claudication.
The definitive treatment for air embolism is thought to be hyperbaric oxygenation (HBO), which is often not available in a timely fashion. Randomized, controlled trials demonstrating efficacy of hyperbaric oxygenation have yet to be performed, but the physiological mode of action seems entirely sufficient to warrant the application of HBO, despite this lack of research.72 Hyperbaric oxygenation will reduce the bubble size (according to Boyle's law), increase tissue oxygenation, and increase the solubility of the gas. The US Navy Dive Table 6 and 6a protocols for gas embolism and decompression sickness would be a good clinical start. (Table 8) Consultation with an experienced hyperbaric physician or dive physician is appropriate for all HBO patients.
Blast injury of the gastrointestinal tract can be managed in much the same way as blunt trauma of the abdomen. If the patient has an obvious penetrating wound of the abdomen, then urgent surgical management is indicated. If the patient is not conscious and hemodynamically unstable, or conscious with abdominal complaints and hemodynamically unstable, then fluid resuscitation should be undertaken. If the patient's blood pressure stabilizes and remains stable, then a noncontrast CT scan of the abdomen is appropriate. If the blood pressure does not improve, then urgent surgical management is indicated. Fatal splenic rupture has been reported in at least 1 victim who had no sign of external injury.73 This suggests a role for FAST ultrasonography in symptomatic patients, or for those patients who cannot be adequately evaluated.
While abdominal CT scan is appropriately specific, older scanners may not be sufficiently sensitive to identify hollow viscus injury.40 If patients who have been scanned continue to have signs of abdominal pathology, then a repeat FAST examination followed by diagnostic peritoneal lavage (DPL) is appropriate. If the DPL effluent contains significant red blood cells, bacteria, bile, or fecal matter, then urgent laparotomy is indicated. CT must precede DPL, or false-positive air and fluid will be introduced.
In the context of a mass casualty incident, there should be a low threshold for laparotomy when a hollow viscus injury is suspected. Close observation may not be possible, because of the number of casualties. Clinical signs and symptoms of early bowel injury, particularly in children, may be so subtle as to be easily missed in the patient with multiple injuries.74
There is about an 80% rate of infection when fragment wounds are sutured. For lacerations and fragment wounds, avoid primary closure and consider the use of delayed primary closure in these wounds.61 Delayed primary closure is the technique of cleaning the wound, leaving the wound open under a moist dressing for approximately 4 to 5 days, and then suturing the wound if there is no evidence of infection. The first step in delayed primary closure is thorough cleansing and removal of debris and devitalized tissue. Heavily contaminated wounds resulting from high-energy missile injuries are ideal for delayed primary closure.
All debris that is flung by the explosion is not radiopaque, and the wise provider should carefully explore injuries and consider CT, ultrasound, or MRI of wounds to evaluate for radiolucent foreign bodies. Update the tetanus status, as appropriate. (For an evidence-based approach to wound care, see Emergency Medicine PRACTICE, Volume 7, Number 3, Wound Care: Modern Evidence In The Treatment Of Man's Age-Old Injuries, March 2005.)
Minimize the physical activity of blast victims after an explosion. Exertion after the blast explosion can increase the severity of primary blast injury. This was seen in WWII, where some blast casualties appeared well, but died after vigorous exercise.28,54
If the patient requires immediate anesthesia for any reason, the patient needs a chest x-ray to look for any evidence of barotrauma. It has been reported that blast victims have a higher morbidity rate when they receive general anesthesia.25 This may well be due to unrecognized primary blast injury and subsequent barotrauma from positive pressure ventilation during anesthesia.25 If barotrauma is noted and the patient requires general anesthesia, bilateral chest tubes are appropriate.24 If possible, local or spinal anesthesia may be better.
New findings based on recent meta-analyses and largescale retrospective studies have disabused us of the notion that a marker for primary blast injury is ear damage (tympanic membrane rupture).30 Both use of hearing protection and partial immersion in water may affect the incidence of ear damage associated with primary blast injury. A recent study showed that primary blast injury is more reliably
associated with skull fractures, burns covering more than 10% of the body surface area, and penetrating injuries to the head or torso.75
Body armor provides a false sense of security during an explosive detonation. The body armor does protect the victim from bomb fragments and, to a lesser extent, objects picked up and flung by the blast wave, but it also provides a reflecting surface that can concentrate the power of the explosion as the blast wave reflects off of the armor front and back.25,27,76,77 (Since the bulk of injuries from an explosive device are from secondary objects flung by the blast wave, the advantages of body armor outweigh the risks of enhancing the blast wave.) The medical provider should not assume that body armor will protect the victim from an explosion-related injury.77
As previously mentioned, a "manufactured" explosive refers to a standard, mass-produced, and quality-tested weapon, while "improvised" describes the use of alternative materials, weapons produced in small quantities, or a device that is used outside of its intended purpose. Improvised explosive devices now found in Iraq are often professional in appearance and operation. These devices have been unexpectedly lethal in action. The emergency physician must not yield to the idea that the "improvised" explosive device is crude and of low efficacy. The rather unwieldy government definition includes professional military devices produced by explosives experts.
When confronted with the scenario that opens this review, you will be facing a busy and very long day. Fortunately, you, your ED, and your hospital have practiced your mass casualty protocols. Rather than being overwhelmed by circumstances, you assume command of the incident within the hospital, and assign your most experienced emergency physician to triage as the casualties start to appear. You point out to the staff that they can expect a high percentage of burns as well as blast injuries, because this is a fuelair explosion (grain dust). You empty all of your ED rooms so that you can start processing the casualties as they arrive. Within 15 minutes of the dispatcher's notification, the first of your reinforcements arrives, and the trauma teams assemble. At the same time, the first of your casualties arrive... in a pickup truck. You thank your lucky stars that this is only a grain elevator, not a terrorist attack.
There are no definitive guidelines for observation, admission, or discharge following ED evaluation for patients with possible blast injury sustained in an explosion. The disposition of these patients depends on the injuries specific to each victim. Those victims with penetrating secondary blast injury or tertiary blast injury need treatment guided by the nature of their injury.
In general, patients with normal chest radiographs and arterial blood gases who have no complaints that would suggest pulmonary blast injury can be considered for discharge after 4-6 hours of observation. Persons exposed to significant closed-space explosions, in-water explosions, and those who were close to the center of the explosion should be considered for observation for at least 8 hours, as they are at higher risk of delayed complications. For those who are sent home, return instructions should include shortness of breath, abdominal pain, vomiting, or development of other symptoms.
Patients with any complaints or findings suspicious for pulmonary or abdominal blast injury should be observed in the hospital. Admit to the hospital all patients with significant burns, abnormal vital signs, abnormal lung examination findings, clinical or radiographic evidence of pulmonary contusion or pneumothorax, abdominal pain, vomiting, evidence of renal contusion, or penetrating injuries to the thorax, abdomen, neck, or cranial cavity. Patients with only penetrating injuries to the extremities should be admitted or discharged, as appropriate to the clinical situation. Patients diagnosed with pulmonary or abdominal blast injury may require complex management and should be admitted to an intensive care unit. Patients with penetrating wounds to head, chest, and abdomen must be treated in accordance with their wounds and good surgical practice.
Transfer of the patient to another medical facility can exacerbate the original injuries. The pulmonary barotrauma from primary blast injury can be exacerbated by air evacuation. As noted earlier, both pneumothorax and arterial gas emboli will enlarge with ascent. All casualties with any evidence of pneumothorax must have a chest tube placed, regardless of the altitude and distance of the flight. Evacuation helicopters should fly at the lowest possible altitude. Long-distance evacuation aircraft should be pressurized to at least 8000 feet (preferably 5000 feet). If the victim has marginal oxygenation (PO2 <60 mm Hg), oxygenation will worsen with ascent in an aircraft. Intubation prior to transport is recommended for all seriously ill patients.
1. "The firefighter wanted to go back and help after he was evaluated in the aid station. He said his buddies were still on the scene and he knew where they were. He had a normal oxygen saturation and had no evidence of external injury ? just a ruptured tympanic membrane. How was I to know he would decompensate?"
2. "The police officer was wearing body armor. She had some injuries on her extremities, but no torso injuries from the fragments. How could I know she was going to develop a pulmonary blast injury?"
3. "The medics on the scene were ignoring the patient who was hypotensive, until she became pulseless and apneic. I thought we could get another save if we could work her up."
4. "How was I to know that she would develop a tension pneumothorax in the helicopter? It seemed like the quickest way to get her to the trauma center."
5. "The bomb went off across the street from the hospital. Many of us went out to bring patients back to the ED. I never even thought about a secondary device ? I just reacted."
Evidence-based medicine requires a critical appraisal of the literature based upon study methodology and number of subjects. Not all references are equally robust. The findings of a large, prospective, randomized, and blinded trial should carry more weight than a case report.
To help the reader judge the strength of each reference, pertinent information about the study, such as the type of study and the number of patients in the study, will be included in bold type following the reference, where available. In addition, the most informative references.
Charles Stewart
April 1, 2006
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